This study aimed to assess tuning the microglia to produce interferon beta (IFN-β) as an anti-inflammatory cytokine through TLR4 pathway in a rat model of AD.
Moreover, in parallel with reducing apoptosis and neural loss in the hippocampal subfields, IFNβ decreased ectopic neurogenesis in the CA1 and CA3 regions of the AD rat hippocampus.
Interestingly, treatment of AD-modeled rats with IFNβ ameliorated memory impairments possibly through suppressing gliosis and shifting from pro-inflammatory toward anti-inflammatory status, suggesting that IFNβ may be a promising therapeutic agent to improve cognitive functions and modulate inflammatory responses in an AD-like neurodegenerative context.
Increased expression of interferon beta (IFN-β) and interferon regulatory factor (IRF)-3 mRNA, two factors induced by TLR-3 signaling, were detected in the AD cases.
This study was designed to investigate whether pretreatment with the TLR2 receptor ligand can regulate microglia to produce interferon β (INFβ) in a rat model of Alzheimer's disease.